Effects of proximal gastrectomy with narrow gastric tube anastomosis compared with total gastrectomy with Roux-en-Y anastomosis on upper gastric cancer.

OBJECTIVE: To investigate the clinical efficacy of proximal gastrectomy with narrow gastric tube anastomosis (PG-NGT) and total gastrectomy with Roux-en-Y anastomosis (TG-RY) for upper gastric cancer. MATERIALS AND METHODS: One hundred sixty-three upper gastric cancer patients were enrolled into the PG-NGT group and TG-RY group. The propensity score matching method was used to conduct a one-to-one match between the two groups with 38 patients in each group. RESULTS: Compared with the TG-RY group, the PG-NGT group had significantly (P < 0.05) shorter operation time, shorter hospital stay, and less intraoperative blood loss. The TG-RY group had significantly (P = 0.009) more lymph nodes dissected and greater (P = 0.014) total cost than the PG-NGT group, but no significant difference existed in the surgical cost between the two groups (P = 0.214). There was no significant (P > 0.05) difference in the incidence of anastomotic stenosis (10.5% vs. 13.1%) or the reflux esophagitis rate (8.6% vs. 9.1%) in the PG-NGT group and the TG-RY group. One year after surgery, the weight and hemoglobin and albumin levels in the PG-NGT group were significantly (P < 0.05) higher than those in the TG-RY group. CONCLUSIONS: PG-NGT may be better than TG-RY in improving patient weight loss and hemoglobin and albumin levels, without increasing the rate of anastomotic stenosis and reflux symptoms.

Upregulation of miR-133a-3p enhances Bufothionine-induced gastric cancer cell death by modulating IGF1R/PI3K/Akt signal pathway mediated ER stress.

AIMS: Bufothionine had been used for gastric cancer (GC) treatment, and this study managed to uncover the underlying mechanisms. MATERIALS AND METHODS: Cell proliferation was determined by CCK-8 assay and colony formation assay. Flow cytometry (FCM) and TUNEL assay were used to measure cell apoptosis ratio. Intracellular ROS was measured by DCFH-DA probes. qRT-PCR was used to determine miRNAs levels. Western Blot was performed to probe proteins. Dual-luciferase reporter gene system was employed to validate the binding sites of miR-133a-3p and 3'UTR regions of IGF1R mRNA. Immunohistochemistry (IHC) was used to determine the expressions of Ki-67 in mice tumor tissues. KEY FINDINGS: Bufothionine inhibited cell viability, triggered ER stress and promoted ROS production in GC cells, and both ER stress inhibitor Salburinal (Sal) and ROS scavenger (NAC) abrogated Bufothionine induced GC cell death. Besides, miR-133a-3p was upregulated by Bufothionine, and Bufothionine-induced cell death was enhanced by miR-133a-3p overexpression while alleviated by miR-133a-3p knockdown. Furthermore, miR-133a-3p inactivated PI3K/Akt signal pathway by sponging IGF1R, and Bufothionine inhibited insulin-like growth factor 1 receptor (IGF1R) and inactivated PI3K/Akt cascade by upregulating miR-133a-3p. Notably, the promoting effects of overexpressed miR-133a-3p on Bufothionine-induced GC cell death were abrogated by overexpressing IGF1R, and aggravated by the PI3K/Akt cascade inhibitor (LY294002). SIGNIFICANCE: Bufothionine promoted GC cell death by triggering miR-133a-3p/IGF1R/PI3K/Akt axis mediated ER stress and ROS production.